Atherosclerosis Smooth muscle proliferation

Atherosclerosis. A type of arteriosclerosis that is characterized by atheroma formation. It is a multifactorial process leading to the accumulation of lipids within the vessel wall, associated with mononuclear cell infiltration and smooth muscle proliferation. Autoimmune-mediated inflammation may play an important role in accelerated atherosclerosis in autoimmune rheumatic diseases. 

A more frequent complication is restenosis of the angioplasty site which occurs in 25-30% of patients over 6-9 months " . Pathological studies in patients with recurrence of symptoms are infrequent but demonstrate proliferation of fibroblasts and vascular smooth muscle cells overlying and distinct from the traumatized atherosclerotic plaque . Similar lesions have been described in early atherosclerosis and there is evidence to suggest a role for platelets in the development of such lesions , possibly through release of platelet-derived growth factors which stimulate fibroblast and vascular smooth muscle proliferation . Thus, depletion or inhibition of platelets prevents the development of atherosclerosis in animal models and aspirin inhibits the accelerated coronary atherosclerosis which occurs in cardiac transplant recipients. Furthermore, restenosis is more frequent when there is evidence of a thrombus at the angioplasty site consistent with previous... 

Atherosclerosis is the primary cause of coronary heart disease, which is characterized by a narrowing (stenosis) of the arteries that supply blood to tissues of the heart [137-139]. Metallic coronary stents were originally developed to prevent abrupt artery closure and to reduce the likelihood of restenosis, which is associated with percutaneous transluminal coronary angioplasty. They are, however, limited by the frequent occurrence of restenosis, which is caused by smooth muscle proliferation, and associated neointimal hyperplasia and target lesion revascularizatiOT [140]. 

Akishita M, Ouchi Y, Miyoshi H, Kozaki K, Inoue S, Ishikawa M, Eto M, Toba K, Orimo H (1997) Estrogen inhibits cuff-induced intimal thickening of rat femoral artery effects on migration and proliferation of vascular smooth muscle cells. Atherosclerosis 130 1-10... 

JLompre I would like to present some of our results describing the changes that occur to cells in culture. My concern is primarily with the organization of the SR when vascular smooth muscle cells proliferate in culture. This is of interest because of the importance of smooth muscle cell proliferation in atherosclerosis and restenosis. Freshly dissociated cells or those that have been cultured for just one... 

Brigehus-Flohe,R., Maurer, S., Lotzer, K., Bol, G., Kalhonpaa, H., Lehtolainen, P., Viita, H., and Yla-Herttuala, S., 2000, Overexpression ofPHGPx inhibits hydroperoxide-induced oxidation, NFkappaB activation and apoptosis and affects oxLDL-mediated proliferation of rabbit aortic smooth muscle cells, Atherosclerosis 152 307-316. 

Homocysteine blood levels (>15 jtmol/L) promote atherosclerosis, perhaps by stimulating proliferation of arterial wall smooth muscle cells. Supplementing the diet with folic acid can reduce high levels. Lpa is a mod-ihed LDL particle that is both atherogenic and pro-thrombic. 

In an effort to investigate antioxidant constituents with antiproliferative effects in rat vascular smooth muscle cells (VSMC), broussoflavan A (36) [49], broussoflavonols F (45) [50] and G (46) [51], and broussoaurone A (48) [49] were found to inhibit the Fe2+-induced thiobarbituric acid-reactive substance formation in rat brain homogenate. Furthermore, broussoflavonols F (45) and G (46) inhibited fetal calf serum-, 5-hydroxytryptamine-, or ADP-induced [3H]thymidine incorporation into rat VSMC [45]. Antioxidant activities and inhibitory effects on proliferation of rat VSMC with potent antiplatelet activities of 45 and 46 may be useful for vascular diseases and atherosclerosis [43,45]. 

Atorvastatin calcium possesses an anti-inflammatory property and reduces the accumulation of inflammatory cells in the atherosclerotic plaques. The drug also inhibits the vascular smooth muscle cell proliferation a key event in the atherogenesis. Atorvastatin also inhibits the platelet function, thereby limiting both the atherosclerosis and the superadded thrombosis and also improves the vascular endothelial function, largely through the amplification of nitric oxide (NO) generation [3-5]. 

The thrombotic disorders include atherothrombosis, endothelial dysfunction, hypercoagulable states, and the thrombophilias. Atherothrombosis or atherosclerosis is a systemic disease of the vessel wall occuring in the aorta, carotid, coronary, and peripheral arteries. The associated inflammatory response is mediated by macrophages and T-lymphocytes with continued smooth muscle cell proliferation, The levels of endothelin-l (ET-I), an extremely potent... 

Leukotrienes increase vascular permeability, wall recruitment of leukocytes, endothelial-cell dysfunction, proliferation of smooth-muscle cells, immune reactivity and mediated vascular inflammation, and atherosclerosis (43). 

The oxidized LDL might damage cells which connect the blood vessel walls by stimulating numerous responses including inflammation, smooth muscle cell proliferation and clotting mechanisms, all of which might lead to atherosclerosis. 

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